An environmental justice analysis of air pollution emissions in the United States from 1970 to 2010.

Over the last decades, air pollution emissions have decreased substantially; however, inequities in air pollution persist. We evaluate county-level racial/ethnic and socioeconomic disparities in emissions changes from six air pollution source sectors (industry [SO2], energy [SO2, NOx], agriculture [NH3], commercial [NOx], residential [particulate organic carbon], and on-road transportation [NOx]) in the contiguous United States during the 40 years following the Clean Air Act (CAA) enactment (1970-2010). We calculate relative emission changes and examine the differential changes given county demographics using hierarchical nested models. The results show racial/ethnic disparities, particularly in the industry and energy generation source sectors. We also find that median family income is a driver of variation in relative emissions changes in all sectors-counties with median family income >$75 K vs. less generally experience larger relative declines in industry, energy, transportation, residential, and commercial-related emissions. Emissions from most air pollution source sectors have, on a national level, decreased following the United States CAA. In this work, we show that the relative reductions in emissions varied across racial/ethnic and socioeconomic groups.

Applying principal component pursuit to investigate the association between source-specific fine particulate matter and myocardial infarction hospitalizations in New York City.

The association between fine particulate matter (PM2.5) and cardiovascular outcomes is well established. To evaluate whether source-specific PM2.5 is differentially associated with cardiovascular disease in New York City (NYC), we identified PM2.5 sources and examined the association between source-specific PM2.5 exposure and risk of hospitalization for myocardial infarction (MI). Methods: We adapted principal component pursuit (PCP), a dimensionality-reduction technique previously used in computer vision, as a novel pattern recognition method for environmental mixtures to apportion speciated PM2.5 to its sources. We used data from the NY Department of Health Statewide Planning and Research Cooperative System of daily city-wide counts of MI admissions (2007-2015). We examined associations between same-day, lag 1, and lag 2 source-specific PM2.5 exposure and MI admissions in a time-series analysis, using a quasi-Poisson regression model adjusting for potential confounders. Results: We identified four sources of PM2.5 pollution: crustal, salt, traffic, and regional and detected three single-species factors: cadmium, chromium, and barium. In adjusted models, we observed a 0.40% (95% confidence interval [CI]: -0.21, 1.01%) increase in MI admission rates per 1 µg/m3 increase in traffic PM2.5, a 0.44% (95% CI: -0.04, 0.93%) increase per 1 µg/m3 increase in crustal PM2.5, and a 1.34% (95% CI: -0.46, 3.17%) increase per 1 µg/m3 increase in chromium-related PM2.5, on average. Conclusions: In our NYC study, we identified traffic, crustal dust, and chromium PM2.5 as potentially relevant sources for cardiovascular disease. We also demonstrated the potential utility of PCP as a pattern recognition method for environmental mixtures.

Exploring Relevant Time Windows in the Association Between PM2.5 Exposure and Amyotrophic Lateral Sclerosis: A Case-Control Study in Denmark.

Studies suggest a link between particulate matter less than or equal to 2.5 µm in diameter (PM2.5) and amyotrophic lateral sclerosis (ALS), but to our knowledge critical exposure windows have not been examined. We performed a case-control study in the Danish population spanning the years 1989-2013. Cases were selected from the Danish National Patient Registry based on International Classification of Diseases codes. Five controls were randomly selected from the Danish Civil Registry and matched to a case on vital status, age, and sex. PM2.5 concentration at residential addresses was assigned using monthly predictions from a dispersion model. We used conditional logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs), adjusting for confounding. We evaluated exposure to averaged PM2.5 concentrations 12-24 months, 2-6 years, and 2-11 years pre-ALS diagnosis; annual lagged exposures up to 11 years prediagnosis; and cumulative associations for exposure in lags 1-5 years and 1-10 years prediagnosis, allowing for varying association estimates by year. We identified 3,983 cases and 19,915 controls. Cumulative exposure to PM2.5 in the period 2-6 years prediagnosis was associated with ALS (OR = 1.06, 95% CI: 0.99, 1.13). Exposures in the second, third, and fourth years prediagnosis were individually associated with higher odds of ALS (e.g., for lag 1, OR = 1.04, 95% CI: 1.00, 1.08). Exposure to PM2.5 within 6 years before diagnosis may represent a critical exposure window for ALS.

Principal Component Pursuit for Pattern Identification in Environmental Mixtures.

BACKGROUND: Environmental health researchers often aim to identify sources or behaviors that give rise to potentially harmful environmental exposures. OBJECTIVE: We adapted principal component pursuit (PCP)-a robust and well-established technique for dimensionality reduction in computer vision and signal processing-to identify patterns in environmental mixtures. PCP decomposes the exposure mixture into a low-rank matrix containing consistent patterns of exposure across pollutants and a sparse matrix isolating unique or extreme exposure events. METHODS: We adapted PCP to accommodate nonnegative data, missing data, and values below a given limit of detection (LOD). We simulated data to represent environmental mixtures of two sizes with increasing proportions

Long-term Traffic-related Air Pollutant Exposure and Amyotrophic Lateral Sclerosis Diagnosis in Denmark: A Bayesian Hierarchical Analysis.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease. Limited evidence suggests ALS diagnosis may be associated with air pollution exposure and specifically traffic-related pollutants. METHODS: In this population-based case-control study, we used 3,937 ALS cases from the Danish National Patient Register diagnosed during 1989-2013 and matched on age, sex, year of birth, and vital status to 19,333 population-based controls free of ALS at index date. We used validated predictions of elemental carbon (EC), nitrogen oxides (NO x ), carbon monoxide (CO), and fine particles (PM 2.5 ) to assign 1-, 5-, and 10-year average exposures pre-ALS diagnosis at study participants' present and historical residential addresses. We used an adjusted Bayesian hierarchical conditional logistic model to estimate individual pollutant associations and joint and average associations for traffic-related pollutants (EC, NO x , CO). RESULTS: For a standard deviation (SD) increase in 5-year average concentrations, EC (SD = 0.42 µg/m 3 ) had a high probability of individual association with increased odds of ALS (11.5%; 95% credible interval [CrI] = -1.0%, 25.6%; 96.3% posterior probability of positive association), with negative associations for NO x (SD = 20 µg/m 3 ) (-4.6%; 95% CrI = 18.1%, 8.9%; 27.8% posterior probability of positive association), CO (SD = 106 µg/m 3 ) (-3.2%; 95% CrI = 14.4%, 10.0%; 26.7% posterior probability of positive association), and a null association for nonelemental carbon fine particles (non-EC PM 2.5 ) (SD = 2.37 µg/m 3 ) (0.7%; 95% CrI = 9.2%, 12.4%). We found no association between ALS and joint or average traffic pollution concentrations. CONCLUSIONS: This study found high probability of a positive association between ALS diagnosis and EC concentration. Further work is needed to understand the role of traffic-related air pollution in ALS pathogenesis.

PM2.5 composition and disease aggravation in amyotrophic lateral sclerosis: An analysis of long-term exposure to components of fine particulate matter in New York State.

Long-term exposure to fine particulate matter (PM2.5) has been associated with disease aggravation in amyotrophic lateral sclerosis (ALS). In this study, we characterized long-term exposure to six major PM2.5 components and their individual association with disease aggravation in ALS. Methods: We leveraged 15 years of data from the New York Department of Health Statewide Planning and Research Cooperative System (2000-2014) to calculate annual ALS first hospitalizations in New York State. We used the first hospital admission as a surrogate of disease aggravation and a prediction model to estimate population-weighted annual black carbon, organic matter (OM), nitrate, sulfate, sea salt, and soil concentrations at the county level. We used a multi-pollutant mixed quasi-Poisson model with county-specific random intercepts to estimate rate ratios (RR) of 1-year exposure to each PM2.5 component and disease aggravation in ALS, adjusting for potential confounders. Results: We observed 5,655 first ALS-related hospitalizations. The annual average hospitalization count per county was 6.08 and the average PM2.5 total mass concentration per county was 8.1 µg/m3-below the United States' National Ambient Air Quality Standard of 12 µg/m3. We found a consistent positive association between ALS aggravation and OM (1.17, 95% confidence intervals [CI], 1.11, 1.24 per standard deviation [SD] increase) and a negative association with soil (RR = 0.91, 95% CI, 0.86, 0.97). Conclusion: Our findings suggest that PM2.5 composition may influence its effect on ALS. We found that annual increases in county-level particulate OM may be associated with disease aggravation in ALS, even at PM2.5 levels below current standards.

Methods for Evaluating Environmental Health Impacts at Different Stages of the Policy Process in Cities.

PURPOSE OF REVIEW: Evaluating the environmental health impacts of urban policies is critical for developing and implementing policies that lead to more healthy and equitable cities. This article aims to (1) identify research questions commonly used when evaluating the health impacts of urban policies at different stages of the policy process, (2) describe commonly used methods, and (3) discuss challenges, opportunities, and future directions. RECENT FINDINGS: In the diagnosis and design stages of the policy process, research questions aim to characterize environmental problems affecting human health and to estimate the potential impacts of new policies. Simulation methods using existing exposure-response information to estimate health impacts predominate at these stages of the policy process. In subsequent stages, e.g., during implementation, research questions aim to understand the actual policy impacts. Simulation methods or observational methods, which rely on experimental data gathered in the study area to assess the effectiveness of the policy, can be applied at these stages. Increasingly, novel techniques fuse both simulation and observational methods to enhance the robustness of impact evaluations assessing implemented policies. The policy process consists of interdependent stages, from inception to end, but most reviewed studies focus on single stages, neglecting the continuity of the policy life cycle. Studies assessing the health impacts of policies using a multi-stage approach are lacking. Most studies investigate intended impacts of policies; focusing also on unintended impacts may provide a more comprehensive evaluation of policies.

Social-distancing fatigue: Evidence from real-time crowd-sourced traffic data.

INTRODUCTION: To mitigate the COVID-19 pandemic and prevent overwhelming the healthcare system, social-distancing policies such as school closure, stay-at-home orders, and indoor dining closure have been utilized worldwide. These policies function by reducing the rate of close contact within populations and result in decreased human mobility. Adherence to social distancing can substantially reduce disease spread. Thus, quantifying human mobility and social-distancing compliance, especially at high temporal resolution, can provide great insight into the impact of social distancing policies. METHODS: We used the movement of individuals around New York City (NYC), measured via traffic levels, as a proxy for human mobility and the impact of social-distancing policies (i.e., work from home policies, school closure, indoor dining closure etc.). By data mining Google traffic in real-time, and applying image processing, we derived high resolution time series of traffic in NYC. We used time series decomposition and generalized additive models to quantify changes in rush hour/non-rush hour, and weekday/weekend traffic, pre-pandemic and following the roll-out of multiple social distancing interventions. RESULTS: Mobility decreased sharply on March 14, 2020 following declaration of the pandemic. However, levels began rebounding by approximately April 13, almost 2 months before stay-at-home orders were lifted, indicating premature increase in mobility, which we term social-distancing fatigue. We also observed large impacts on diurnal traffic congestion, such that the pre-pandemic bi-modal weekday congestion representing morning and evening rush hour was dramatically altered. By September, traffic congestion rebounded to approximately 75% of pre-pandemic levels. CONCLUSION: Using crowd-sourced traffic congestion data, we described changes in mobility in Manhattan, NYC, during the COVID-19 pandemic. These data can be used to inform human mobility changes during the current pandemic, in planning for responses to future pandemics, and in understanding the potential impact of large-scale traffic interventions such as congestion pricing policies.

Parkinson's disease aggravation in association with fine particle components in New York State.

BACKGROUND: Long-term exposure to fine particulate matter (PM2.5) has been associated with neurodegenerative diseases, including disease aggravation in Parkinson's disease (PD), but associations with specific PM2.5 components have not been evaluated. OBJECTIVE: To characterize the association between specific PM2.5 components and PD first hospitalization, a surrogate for disease aggravation. METHODS: We obtained data on hospitalizations from the New York Department of Health Statewide Planning and Research Cooperative System (2000-2014) to calculate annual first PD hospitalization counts in New York State per county. We used well-validated prediction models at 1 km2 resolution to estimate county level population-weighted annual black carbon (BC), organic matter (OM), nitrate, sulfate, sea salt (SS), and soil particle concentrations. We then used a multi-pollutant mixed quasi-Poisson model with county-specific random intercepts to estimate rate ratios (RR) of one-year exposure to each PM2.5 component and PD disease aggravation. We evaluated potential nonlinear exposure-outcome relationships using penalized splines and accounted for potential confounders. RESULTS: We observed a total of 197,545 PD first hospitalizations in NYS from 2000 to 2014. The annual average count per county was 212 first hospitalizations. The RR (95% confidence interval) for PD aggravation was 1.06 (1.03, 1.10) per one standard deviation (SD) increase in nitrate concentrations and 1.06 (1.04, 1.09) for the corresponding increase in OM concentrations. We also found a nonlinear inverse association between PD aggravation and BC at concentrations above the 96th percentile. We found a marginal association with SS and no association with sulfate or soil exposure. CONCLUSION: In this study, we detected associations between the PM2.5 components OM and nitrate with PD disease aggravation. Our findings support that PM2.5 adverse effects on PD may vary by particle composition.

Reflection on modern methods: good practices for applied statistical learning in epidemiology.

Statistical learning includes methods that extract knowledge from complex data. Statistical learning methods beyond generalized linear models, such as shrinkage methods or kernel smoothing methods, are being increasingly implemented in public health research and epidemiology because they can perform better in instances with complex or high-dimensional data-settings in which traditional statistical methods fail. These novel methods, however, often include random sampling which may induce variability in results. Best practices in data science can help to ensure robustness. As a case study, we included four statistical learning models that have been applied previously to analyze the relationship between environmental mixtures and health outcomes. We ran each model across 100 initializing values for random number generation, or 'seeds', and assessed variability in resulting estimation and inference. All methods exhibited some seed-dependent variability in results. The degree of variability differed across methods and exposure of interest. Any statistical learning method reliant on a random seed will exhibit some degree of seed sensitivity. We recommend that researchers repeat their analysis with various seeds as a sensitivity analysis when implementing these methods to enhance interpretability and robustness of results.

Social-distancing Fatigue: Evidence from Real-time Crowd-sourced Traffic Data.

INTRODUCTION: To mitigate the COVID-19 pandemic and prevent overwhelming the healthcare system, social-distancing policies such as school closure, stay-at-home orders, and indoor dining closure have been utilized worldwide. These policies function by reducing the rate of close contact within populations and results in decreased human mobility. Adherence to social distancing can substantially reduce disease spread. Thus, quantifying human mobility and social-distancing compliance, especially at high temporal resolution, can provide great insight into the impact of social distancing policies. METHODS: We used the movement of individuals around New York City (NYC), measured via traffic levels, as a proxy for human mobility and the impact of social-distancing policies (i.e., work from home policies, school closure, indoor dining closure etc.). By data mining Google traffic in real-time, and applying image processing, we derived high resolution time series of traffic in NYC. We used time series decomposition and generalized additive models to quantify changes in rush hour/non-rush hour, and weekday/weekend traffic, pre-pandemic and following the roll-out of multiple social distancing interventions. RESULTS: Mobility decreased sharply on March 14, 2020 following declaration of the pandemic. However, levels began rebounding by approximately April 13, almost 2 months before stay-at-home orders were lifted, indicating premature increase in mobility, which we term social-distancing fatigue. We also observed large impacts on diurnal traffic congestion, such that the pre-pandemic bi-modal weekday congestion representing morning and evening rush hour was dramatically altered. By September, traffic congestion rebounded to approximately 75% of pre-pandemic levels. CONCLUSION: Using crowd-sourced traffic congestion data, we described changes in mobility in Manhattan, NYC, during the COVID-19 pandemic. These data can be used to inform human mobility changes during the current pandemic, in planning for responses to future pandemics, and in understanding the potential impact of large-scale traffic interventions such as congestion pricing policies.

Fine Particle Exposure and Clinical Aggravation in Neurodegenerative Diseases in New York State.

BACKGROUND: Adult-onset neurodegenerative diseases affect millions and negatively impact health care systems worldwide. Evidence suggests that air pollution may contribute to aggravation of neurodegeneration, but studies have been limited. OBJECTIVE: We examined the potential association between long-term exposure to particulate matter ≤2.5µm in aerodynamic diameter [fine particulate matter (PM2.5)] and disease aggravation in Alzheimer's (AD) and Parkinson's (PD) diseases and amyotrophic lateral sclerosis (ALS), using first hospitalization as a surrogate of clinical aggravation. METHODS: We used data from the New York Department of Health Statewide Planning and Research Cooperative System (SPARCS 2000-2014) to construct annual county counts of first hospitalizations with a diagnosis of AD, PD, or ALS (total, urbanicity-, sex-, and age-stratified). We used annual PM2.5 concentrations estimated by a prediction model at a 1-km2 resolution, which we aggregated to population-weighted county averages to assign exposure to cases based on county of residence. We used outcome-specific mixed quasi-Poisson models with county-specific random intercepts to estimate rate ratios (RRs) for a 1-y PM2.5 exposure. We allowed for nonlinear exposure-outcome relationships using penalized splines and accounted for potential confounders. RESULTS: We found a positive nonlinear PM2.5-PD association that plateaued above 11 µg/m3 (RR=1.09, 95% CI: 1.04, 1.14 for a PM2.5 increase from 8.1 to 10.4 µg/m3). We also found a linear PM2.5-ALS positive association (RR=1.05, 95% CI: 1.01, 1.09 per 1-µg/m3 PM2.5 increase), and suggestive evidence of an association with AD. We found effect modification by age for PD and ALS with a stronger positive association in patients <70 years of age but found insufficient evidence of effect modification by sex or urbanization level for any of the outcomes. CONCLUSION: Our findings suggest that annual increase in county-level PM2.5 concentrations may contribute to clinical aggravation of PD and ALS. Importantly, the average annual PM2.5 concentration in our study was 8.1 µg/m3, below the current American national standards, suggesting the standards may not adequately protect the aging population. https://doi.org/10.1289/EHP7425.

An overview of methods to address distinct research questions on environmental mixtures: an application to persistent organic pollutants and leukocyte telomere length.

BACKGROUND: Numerous methods exist to analyze complex environmental mixtures in health studies. As an illustration of the different uses of mixture methods, we employed methods geared toward distinct research questions concerning persistent organic chemicals (POPs) as a mixture and leukocyte telomere length (LTL) as an outcome. METHODS: With information on 18 POPs and LTL among 1,003 U.S. adults (NHANES, 2001-2002), we used unsupervised methods including clustering to identify profiles of similarly exposed participants, and Principal Component Analysis (PCA) and Exploratory Factor Analysis (EFA) to identify common exposure patterns. We also employed supervised learning techniques, including penalized, weighted quantile sum (WQS), and Bayesian kernel machine (BKMR) regressions, to identify potentially toxic agents, and characterize nonlinear associations, interactions, and the overall mixture effect. RESULTS: Clustering separated participants into high, medium, and low POP exposure groups; longer log-LTL was found among those with high exposure. The first PCA component represented overall POP exposure and was positively associated with log-LTL. Two EFA factors, one representing furans and the other PCBs 126 and 118, were positively associated with log-LTL. Penalized regression methods selected three congeners in common (PCB 126, PCB 118, and furan 2,3,4,7,8-pncdf) as potentially toxic agents. WQS found a positive overall effect of the POP mixture and identified six POPs as potentially toxic agents (furans 1,2,3,4,6,7,8-hxcdf, 2,3,4,7,8-pncdf, and 1,2,3,6,7,8-hxcdf, and PCBs 99, 126, 169). BKMR found a positive linear association with furan 2,3,4,7,8-pncdf, suggestive evidence of linear associations with PCBs 126 and 169, and a positive overall effect of the mixture, but no interactions among congeners. CONCLUSIONS: Using different methods, we identified patterns of POP exposure, potentially toxic agents, the absence of interaction, and estimated the overall mixture effect. These applications and results may serve as a guide for mixture method selection based on specific research questions.

Organophosphate neurotoxicity to the voluntary motor system on the trail of environment-caused amyotrophic lateral sclerosis: the known, the misknown, and the unknown.

Amyotrophic lateral sclerosis (ALS) is the most common adult-onset paralytic disorder. It is characterized by progressive degeneration of the motor neurons controlling voluntary movement. The underlying mechanisms remain elusive, a fact that has precluded development of effective treatments. ALS presents as a sporadic condition 90-95% of the time, i.e., without familial history or obvious genetic mutation. This suggests that ALS has a strong environmental component. Organophosphates (OPs) are prime candidate neurotoxicants in the etiology of ALS, as exposure to OPs was linked to higher ALS incidence among farmers, soccer players, and Gulf War veterans. In addition, polymorphisms in paraoxonase 1, an enzyme that detoxifies OPs, may increase individual vulnerability both to OP poisoning and to the risk of developing ALS. Furthermore, exposure to high doses of OPs can give rise to OP-induced delayed neuropathy (OPIDN), a debilitating condition akin to ALS characterized by similar motor impairment and paralysis. The question we pose in this review is: "what can we learn from acute exposure to high doses of neurotoxicants (OPIDN) that could help our understanding of chronic diseases resulting from potentially decades of silent exposure (ALS)?" The resemblances between OPIDN and ALS are striking at the clinical, etiological, neuropathological, cellular, and potentially molecular levels. Here, we critically present available evidence, discuss current limitations, and posit future research. In the search for the environmental origin of ALS, OPIDN offers an exciting trail to follow, which can hopefully lead to the development of novel strategies to prevent and cure these dreadful disorders.

Altered proliferation and networks in neural cells derived from idiopathic autistic individuals.

Autism spectrum disorders (ASD) are common, complex and heterogeneous neurodevelopmental disorders. Cellular and molecular mechanisms responsible for ASD pathogenesis have been proposed based on genetic studies, brain pathology and imaging, but a major impediment to testing ASD hypotheses is the lack of human cell models. Here, we reprogrammed fibroblasts to generate induced pluripotent stem cells, neural progenitor cells (NPCs) and neurons from ASD individuals with early brain overgrowth and non-ASD controls with normal brain size. ASD-derived NPCs display increased cell proliferation because of dysregulation of a ß-catenin/BRN2 transcriptional cascade. ASD-derived neurons display abnormal neurogenesis and reduced synaptogenesis leading to functional defects in neuronal networks. Interestingly, defects in neuronal networks could be rescued by insulin growth factor 1 (IGF-1), a drug that is currently in clinical trials for ASD. This work demonstrates that selection of ASD subjects based on endophenotypes unraveled biologically relevant pathway disruption and revealed a potential cellular mechanism for the therapeutic effect of IGF-1.